The overall objective of current studies is aimed at determining the role of inflammation in the pathogenesis of psoriasis. The current objective is to determine if the epidermis in psoriasis is inherently defective. Prior to starting definitive studies of this type, we have been using pig skin transplanted to the athymic mouse, as a model of xenogeneically grafted skin in which to work out agents which will induce and suppress proliferation of transplanted epidermis. In the past, we have demonstrated that skin from patients with psoriasis can be transplanted to the athymic mouse. This will afford the opportunity to look at the effect of inflammatory mediators separate from humoral mediators usually present in vivo in host afflicted with disease. Our proposal is to generate proliferative events in involved and uninvolved skin of psoriasis patients, transplanted to the athymic mouse. These proliferative events will be followed to determine whether or not there is altered abnormal epidermal homeostasis in the animal model setting. Various humoral mediators will then be added to determine the effect of such biologic mediators on proliferative events.